AI Article Synopsis
- ALS (Amyotrophic Lateral Sclerosis) involves the degeneration of motor neurons, with glial cells playing a significant role in disease progression.
- Research using the hSOD1(G93A) mouse model reveals that interactions between motor neurons and glial cells lead to notable changes in gene expression, proving that these cells influence each other significantly.
- The study finds a strong correlation between lab results (cell cultures) and gene expression in actual spinal tissues during ALS progression, highlighting specific genes and pathways like TGF-β that may contribute to motor neuron degeneration.
Article Abstract
ALS results from the selective and progressive degeneration of motor neurons. Although the underlying disease mechanisms remain unknown, glial cells have been implicated in ALS disease progression. Here, we examine the effects of glial cell/motor neuron interactions on gene expression using the hSOD1(G93A) (the G93A allele of the human superoxide dismutase gene) mouse model of ALS. We detect striking cell autonomous and nonautonomous changes in gene expression in cocultured motor neurons and glia, revealing that the two cell types profoundly affect each other. In addition, we found a remarkable concordance between the cell culture data and expression profiles of whole spinal cords and acutely isolated spinal cord cells during disease progression in the G93A mouse model, providing validation of the cell culture approach. Bioinformatics analyses identified changes in the expression of specific genes and signaling pathways that may contribute to motor neuron degeneration in ALS, among which are TGF-β signaling pathways.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3581928 | PMC |
| http://dx.doi.org/10.1073/pnas.1222361110 | DOI Listing |
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